In FY2008 we focused on the capsid protein of HEV. Although HEV is not an enveloped virus, its closest relative, according to sequence analysis, is rubella virus which is enveloped. Others have reported that the HEV capsid protein was glycosylated when artificially over-expressed from a plasmid vector. Since glycosylation is a hallmark of receptor proteins of enveloped viruses, this result was important to confirm because it has basic implications for HEV replication and pathogenicity. Our studies with infectious HEV replicating naturally in human hepatoma cells failed to find any evidence of glycosylation and suggested that the previous results of others were an artifact of over-expression. We also developed a system which permits trans-encapsidation of HEV genomes and we have begun to use it to characterize the capsid protein structure-function relationships.